Apoptotic Changes in Gingiva Caused by Smoking

Apoptosis and Tissue Destruction in Gingival Tissues of Smoker and Non-smoker Periodontitis Patients

Smoking is a major environmental risk factor associated with common forms of human chronic periodontitis. The aim of the present study was to evaluate apoptotic tissue alterations and tissue destruction in smoker and non-smoker chronic periodontitis patients and healthy individuals. The investigators of the study suggest that smoking decrease tissue quality and increase inflammation level in gingival tissues in both healthy individuals and periodontitis patients. One possible mechanism for this is suggested to be increased apoptosis.

Study Overview

• Status: Completed
• Conditions: Smoking; Chronic Periodontitis

Detailed Description

Periodontal disease disrupts soft tissue metabolism in the gingiva through a decrease in the production of collagen, the quality, and quantity of the connective tissue. The etiology and pathogenesis of chronic periodontitis are mostly revealed, however, the mechanism of environmental factors such as smoking yet to be clarified. Major consequences of smoking in gingival tissues are suggested to be the reduction in neutrophil and fibroblast function, decreased immunoglobulin G production, increased periodontal pathogen bacteria prevalence, difficulty in eliminating pathogens with mechanical therapy, and reduction in growth factor production. In the present study, markers of tissue destruction, matrix metalloproteinase-8 and tissue inhibitor of matrix metalloproteinase-1, hypoxia markers, vascular endothelial growth factor and hypoxia-inducible factor and apoptotic markers, bax, bcl-2, and caspase-3 were evaluated.

• Study Type: Observational
• Enrollment (Actual): 60

Contacts and Locations

Study Locations

• Turkey
  • Tokat, Turkey, 60100
    • Gaziosmanpasa University Faculty of Dentistry

Participation Criteria

Eligibility Criteria

• Ages Eligible for Study: 30 years to 50 years (Adult)
• Accepts Healthy Volunteers: Yes
• Genders Eligible for Study: All

• Sampling Method: Probability Sample

Study Population

Healthy individuals who were either smokers or non-smokers, chronic periodontitis patients who were either smokers or non-smokers older than 30 years old and younger than 50 years old were enrolled. The age was specifically chosen because aging changes periodontal and gingival tissues independently of other variables. Any possible factor which might alter connective tissue metabolism were excluded.

Description

Inclusion Criteria:

• Age range from 30 to 45,
• the existence of at least 20 functioning teeth,
• systemical health,
• no antibiotic use within 6 months,
• no periodontal therapy within 6 months,
• no pregnancy or lactation,
• no drug use, in addition; for the smokers existence of the smoking condition for at least five years.

Exclusion Criteria:

• Patients younger than 30 older than 50 years old,
• the absence of occlusion,
• drug use,
• pregnancy/lactation,
• previous antibiotic use,
• previous periodontal therapy,
• the existence of any systemical disease.

Study Plan

How is the study designed?

Number of groups / cohorts

4

Cohorts and Interventions

Group / Cohort
Healthy individuals; Gingival biopsies of healthy individuals who were never-smokers and had no systemic or oral disease or condition.
periodontitis patients; Gingival biopsies of periodontitis patients who were never-smokers and had no systemic disease or condition.
Healthy smokers; Gingival biopsies of healthy individuals who were smokers but no systemic or oral disease or condition.
Smokers with periodontitis; Gingival biopsies of periodontitis patients who were smokers but no systemic disease or condition.

What is the study measuring?

Primary Outcome Measures

Outcome Measure	Measure Description	Time Frame
Fibroblast and total inflammatory cell counts	Fibroblast and total inflammatory cell counts in the groups were determined in a standardized 1000 micrometer square area with histomorphometric evaluation.	Biopsies were obtained a day after initial examinations, histological analysis were performed 2 weeks after.

Secondary Outcome Measures

Outcome Measure	Measure Description	Time Frame
Apoptotic markers	Apoptotic and anti-apoptotic proteins and enzymes related to apoptosis were evaluated via immunohistochemistry.	Biopsies were obtained a day after initial examinations, histological analysis were performed 2 weeks after
Hypoxia and tissue destruction markers	Vascular endothelial growth factor and hypoxia-inducible factor as hypoxia markers and matrix metalloproteinase and it inhibitor as destruction markers were evaluated via immunohistochemistry.	Biopsies were obtained a day after initial examinations, histological analysis were performed 2 weeks after

Collaborators and Investigators

• Sponsor: Tokat Gaziosmanpasa University
• Investigators: Principal Investigator: HATİCE BALCI YÜCE, PhD, Gaziosmanpasa University

Study record dates

Study Major Dates

• Study Start (Actual): January 10, 2017
• Primary Completion (Actual): January 10, 2018
• Study Completion (Actual): April 10, 2018

Study Registration Dates

• First Submitted: August 13, 2018
• First Submitted That Met QC Criteria: August 13, 2018
• First Posted (Actual): August 15, 2018

Study Record Updates

• Last Update Posted (Actual): August 16, 2018
• Last Update Submitted That Met QC Criteria: August 15, 2018
• Last Verified: August 1, 2018

More Information

Terms related to this study

• Keywords: smoking; hypoxia; apoptosis; chronic periodontitis
• Additional Relevant MeSH Terms: Stomatognathic Diseases; Periodontal Diseases; Mouth Diseases; Periodontitis; Chronic Periodontitis
• Other Study ID Numbers: Özkan

Plan for Individual participant data (IPD)

• Plan to Share Individual Participant Data (IPD)?: UNDECIDED

Drug and device information, study documents

• Studies a U.S. FDA-regulated drug product: No
• Studies a U.S. FDA-regulated device product: No